Chronic autoimmune thyroiditis code according to mcb 10. Autoimmune thyroiditis
ICD systems were adopted more than a hundred years ago at a conference in Paris with the possibility of revising it every 10 years. During its existence, the system has been revised ten times.
Since 1993, code ten began to operate, which includes thyroid diseases such as chronic autoimmune thyroiditis. The main purpose of the ICD application was the definition of pathologies, their analysis and comparison of the data obtained in different countries of the world. Also, this classification allows you to select the most effective treatment regimens for pathologies included in the code.
All data on pathologies are formed in such a way as to create the most useful database of diseases, useful for epidemiology, practical medicine.
The following groups of pathologies are included in the ICD-10 code:
- diseases of an epidemic nature;
- common diseases;
- diseases grouped by anatomical localization;
- developmental pathology;
- different types of herbs.
This code contains more than 20 groups, among them group IV, which includes diseases of the endocrine system and metabolism.
Autoimmune thyroiditis code for microbial 10 is included in the group of thyroid diseases. To record pathologies, codes from E00 to E07 are used. The E06 code reflects the pathology of thyroiditis.
This includes the following subsections:
- E06-0 code. This code designates the acute course of thyroiditis.
- E06-1. This includes subacute thyroiditis mcb 10.
- E06-2. Chronic form of thyroiditis.
- Icb classifies autoimmune thyroiditis as E06-3.
- E06-4. Medication-induced thyroiditis.
- E06-5. Other types of thyroiditis.
Autoimmune thyroiditis is a dangerous genetic disorder that is manifested by a decrease in thyroid hormones. There are two types of pathology, indicated by one code.
These are Hashimoto's chronic autoimmune thyroiditis and Riedel's disease. With the latter variant of the disease, the thyroid parenchyma is replaced by connective tissue.
The international code allows you to determine not only the disease, but also to learn about the clinical manifestations of pathologies, as well as to determine the methods of diagnosis and treatment.
If symptoms of hypothyroidism are detected, Hashimoto's disease should be assumed. To clarify the diagnosis, a blood test for TSH and T4 is performed. If laboratory diagnostics show the presence of antibodies to thyroglobulin, then this will speak of the autoimmune nature of the disease.
Ultrasound will help to clarify the diagnosis. During this examination, the doctor may see hyperechoic layers, connective tissue, and accumulations of lymphoid follicles. For a more accurate diagnosis, a cytological examination should be carried out, since on an ultrasound scan, the pathology of E06-3 is similar to a malignant formation.
Treatment for E06-3 involves lifelong hormone intake. In rare cases, surgery is indicated.
iCD 10 code is the name of a disease in the worldwide classification of diseases. The ICD is a huge system that was created in order to study diseases in detail and track the trend in the incidence of the population. This classification was adopted more than a century ago in Paris, however, it is changed and supplemented every 10 years.
The code ten appeared in 1993 and characterized a thyroid disease, namely chronic autoimmune thyroiditis. The meaning of the ICD was to identify complex pathologies and carry out diagnostics, which were subsequently compared in many countries of the world. Thanks to this classification, an optimal system for the treatment of all pathologies has been developed. Each has its own code according to the ICD 10 system.
All disease information has been compiled in such a way that it can be used to compile the most useful database. The ICD 10 code contains the following pathologies:
- diseases of an epidemic nature;
- common diseases;
- diseases associated with anatomical localization;
- developmental pathology;
- various types of injuries.
The code contains over twenty groups. Autoimmune thyroiditis is contained in the group of thyroid dysfunction and includes the following disease codes:
- acute, which is designated by the code E06.0 - it is characterized by a thyroid abscess and is divided into purulent and pyogenic. Sometimes other codes are applied to it, namely B95, B96, B97;
- subacute has encryption E06.1 and is divided into de Quervain's thyroiditis, giant (cellular), granular and without pus;
- chronic often turns into thyrotoxicosis and is designated as E06.2;
- autoimmune, which is divided into 4 subspecies: Hashimoto's disease Hasitotoxicosis (also called transient), lymphadenomatous goiter, lymphocytic thyroiditis, lymphomatous struma;
- medicinal, encrypted as E06.4, but other encodings are used if necessary;
- ordinary, which includes chronic, woody, fibrious, Riedel's thyroiditis and NOS. Bears code E06.5;
- unspecified, code E06.9.
Hashimoto's disease is a pathology that occurs when hormone levels fall rapidly, which occurs due to a reduction in the volume of hormone-producing tissue.
Riedel's disease, or as it is also called fibrious, is chronic. Its feature is the replacement of the parenchyma with another type of tissue (connective).
And if the Hashimoto subspecies appears very often, then the Riedel subspecies, on the contrary, is very rare.
With the first disease, the disease mainly affects women over the age of thirty-five. It appears like this: the normal tissues of the thyroid gland disintegrate, and new ones appear in their place.
In other words, due to autoimmune aggression, diffuse infiltration of the thyroid gland by lymphocytes occurs with the formation of lymphoid follicles (lymphocytic thyroiditis), destruction of thyrocytes and proliferation of fibrous tissue.
The transition phase of hyperthyroidism is closely interrelated with the non-functionality of healthy epithelial cells of the follicle and the ingestion of long-synthesized hormones into the human blood. In the future, this leads to the occurrence of hypothyroidism.
In the second subspecies of the disease, the healthy parenchyma changes to fibrious tissue, which causes the compression syndrome. This type is very often interconnected with different types of fibriosis, namely mediastinal and retroperitoneal, which makes it possible to study it within the framework of Ormond's systemic fibrosing syndrome. There is an opinion that Riedel's thyroiditis is the outcome of Hashimoto's thyroiditis.
Hashimoto's disease is divided into two forms of pathology development - hypertrophic and atrophic. The first form is explicit, and the second is latent.
First of all, it is necessary to conduct an examination for Hashimoto's thyroiditis when the following symptoms appear in a woman aged 35-40 years:
- hair began to fall out;
- breaking nails;
- face swelling appears;
- dry skin.
To do this, you need to donate blood for T and TSH analysis. And also the doctor determines by touch whether the lobes of the thyroid gland are enlarged and they are asymmetric or not. When conducting an ultrasound examination, the general picture of the disease is very similar to DTZ - the tissue has many layers and pseudo-nodes.
If Riedel is diagnosed, then the thyroid gland will be very dense and involve neighboring organs in the disease. This disease is difficult to distinguish from thyroid cancer.
With autoimmune thyroiditis, the ICD code 10 is prescribed lifelong hormone therapy. The operation is prescribed in individual cases (large goiter, malignant tumor).
ICD-10 / E00-E90 CLASS IV Diseases of the endocrine system, eating disorders and metabolic disorders / E00-E07 Diseases of the thyroid gland / E06 Thyroiditis
Hashimoto's thyroiditis
In 2-4% of patients, the thyrotoxic form of chronic lymphocytic thyroiditis (hashitoxicosis, Hashimoto's goiter) occurs.
In some of these patients, on initial examination, an unusually dense goiter and high titers of antithyroid autoantibodies are found. Such patients are characterized by mild or moderate thyrotoxicosis caused by thyroid-stimulating autoantibodies. It is assumed that the thyrotoxic form of the disease is a combination of chronic lymphocytic thyroiditis and diffuse toxic goiter. In other patients in this group, thyrotoxicosis develops against the background of previous hypothyroidism. Probably, in such cases, thyrotoxicosis is caused by the newly emerging clones of B-lymphocytes secreting thyroid-stimulating autoantibodies.
Autoimmune Thyroiditis: Diagnosis
Laboratory and instrumental research
In about 80% of patients with chronic lymphocytic thyroiditis, at the time of diagnosis, the levels of total T4, total T3 and TSH in serum are normal, but the secretory function of the thyroid gland is reduced. This is indicated by an increase in TSH secretion in a test with thyroliberin (this test is optional to establish a diagnosis of chronic lymphocytic thyroiditis). More than 85% of patients with chronic lymphocytic thyroiditis have autoantibodies to thyroglobulin, microsomal antigens and iodide peroxidase. These autoantibodies are also found in other diseases of the thyroid gland (for example, in 80% of patients with diffuse toxic goiter), but in chronic lymphocytic thyroiditis, their titer is usually higher. A significant increase in the titer of autoantibodies is often found in patients with primary thyroid lymphoma. It is assumed that the mechanisms of autoimmune reactions in chronic lymphocytic thyroiditis and in lymphoma are similar. A growing hard goiter in an elderly patient may be a sign of lymphoma and warrants a thyroid biopsy if anti-thyroid autoantibodies are found.
Thyroid scintigraphy usually reveals a symmetrical enlargement with an uneven distribution of the isotope. Sometimes a single cold knot is visualized. The uptake of radioactive iodine by the thyroid gland can be normal, decreased, or increased. It should be noted that thyroid scintigraphy and a test with the absorption of radioactive iodine with suspected chronic lymphocytic thyroiditis have little diagnostic value. However, the value of the results of these tests increases if a single nodule is found in the thyroid gland or if thyroid enlargement continues despite thyroid hormone treatment. In these cases, a fine-needle biopsy of the node or enlarging area is performed to exclude neoplasm.
Autoimmune Thyroiditis: Treatment
Prevention
Other
Chronic lymphocytic thyroiditis
Etiology and pathogenesis
Chronic lymphocytic thyroiditis is an organ-specific autoimmune disease. It is believed that its main cause is a defect in CD8 lymphocytes (T-suppressors), due to which CD4 lymphocytes (T-helpers) are able to interact with antigens of thyroid cells. In patients with chronic lymphocytic thyroiditis, HLA-DR5 is often found, which indicates a genetic predisposition to this disease. Chronic lymphocytic thyroiditis can be combined with other autoimmune diseases (see Table 28.5).
Clinical manifestations
The disease is most often diagnosed in middle-aged women with asymptomatic goiter. Women make up approximately 95% of patients. Clinical manifestations are diverse: from a small goiter without symptoms of hypothyroidism to myxedema. The earliest and most characteristic sign of the disease is an enlarged thyroid gland. Common complaints are pressure, tension, or pain on the front of the neck. Mild dysphagia or hoarseness is sometimes observed. Unpleasant sensations on the front of the neck can be caused by a rapid enlargement of the thyroid gland, but more often it enlarges gradually and without symptoms. The clinical picture at the time of examination is determined by the functional state of the thyroid gland (the presence of hypothyroidism, euthyroidism or thyrotoxicosis). Symptoms of hypothyroidism appear only when T4 and T3 levels are significantly reduced.
Diagnostics
On physical examination, a symmetrical, very dense, mobile goiter is usually found, often of an uneven or nodular consistency. Sometimes a single node is palpated in the thyroid gland.
Elderly patients (average age 60 years) sometimes have an atrophic form of the disease - primary idiopathic hypothyroidism. In such cases, goiter is usually absent, and the deficiency of thyroid hormones is manifested by lethargy, drowsiness, hoarseness, facial swelling, and bradycardia. It is believed that primary idiopathic hypothyroidism is caused by thyroid-blocking autoantibodies or destruction of thyrocytes by cytotoxic antithyroid autoantibodies.
1. Nikolai TF, et al. Postpartum lymphocytic thyroiditis: Prevalence, clinical course, and long-term follow-up. Arch Intern Med 147: 221, 1987.
2. Nyulassy S, et al. Subacute (de Quervain) thyroiditis: Association with HLA-B35 antigen and abnormalities of the complement system immunoglobulins and other serum proteins. J Clin Endocrinol Metab 45: 270, 1977.
3. Vargas MT, et al. Antithyroid microsomal autoantibodies and HLA-DR5 are associated with postpartum thyroid dysfunction: Evidence supporting an autoimmune pathogenesis. J Clin Endocrinol Metab 67: 327, 1988.
4. Volpe R. Is silent thyroiditis an autoimmune disease? Arch Intern Med 148: 1907, 1988.
Pathogenesis of autoimmune thyroiditis
The reasons for the organ-specific autoimmune process in this pathology are the perception by the immune system of the body of the thyroid cells as foreign antigens and the production of antibodies against them. Antibodies begin to "work", and T-lymphocytes (which must recognize and destroy foreign cells) rush into the tissue of the gland, triggering inflammation - thyroiditis. In this case, effector T-lymphocytes penetrate into the parenchyma of the thyroid gland and accumulate there, forming lymphocytic (lymphoplasmacytic) infiltrates. Against this background, the tissues of the gland undergo destructive changes: the integrity of the membranes of the follicles and the walls of thyrocytes (follicular cells that produce hormones) is disrupted, part of the glandular tissue can be replaced by fibrous tissue. Follicular cells, naturally, are destroyed, their number is reduced, and as a result, thyroid dysfunction occurs. This leads to hypothyroidism - a lowered level of thyroid hormones.
But this does not happen immediately, the pathogenesis of autoimmune thyroiditis is characterized by a long asymptomatic period (euthyroid phase), when the levels of thyroid hormones in the blood are within normal limits. Further, the disease begins to progress, causing hormone deficiency. The pituitary gland, which controls the work of the thyroid gland, reacts to this and, by increasing the synthesis of thyroid-stimulating hormone (TSH), for some time stimulates the production of thyroxine. Therefore, months or even years may pass until the pathology becomes apparent.
The predisposition to autoimmune diseases is determined by an inherited dominant genetic trait. Studies have shown that in half of the immediate family of patients with autoimmune thyroiditis, antibodies on the thyroid tissue are also present in the blood serum. To date, scientists associate the development of autoimmune thyroiditis with mutations in two genes - 8q23-q24 on chromosome 8 and 2q33 on chromosome 2.
As endocrinologists note, there are immune diseases that cause autoimmune thyroiditis, more precisely, combined with it: type I diabetes, celiac disease (celiac disease), pernicious anemia, rheumatoid arthritis, systemic lupus erythematosus, Addison's disease, Verlhof's disease, primary biliary cirrhosis , as well as Down syndrome, Shereshevsky-Turner and Klinefelter syndromes.
In women, autoimmune thyroiditis occurs 10 times more often than in men, and usually manifests itself after 40 years (according to The European Society of Endocrinology, the typical age of onset of the disease is 35-55 years). Despite the hereditary nature of the disease, autoimmune thyroiditis is almost never diagnosed in children under 5 years old, but already in adolescents it accounts for up to 40% of all thyroid pathologies.
Included: endemic conditions associated with iodine deficiency in the natural environment, both directly and as a result of iodine deficiency in the mother's body. Some of these conditions cannot be considered true hypothyroidism, but are the result of inappropriate secretion of thyroid hormones in the developing fetus; there may be a connection with natural goitrogenic factors. If necessary, to identify concomitant mental retardation, use an additional code (F70-F79). Excluded: subclinical hypothyroidism due to iodine deficiency (E02)
- E00.0 Congenital iodine deficiency syndrome, neurological form. Endemic cretinism, neurological form
- E00.1 Congenital iodine deficiency syndrome, myxedema form Endemic cretinism: hypothyroid, myxedema form
- E00.2 Congenital iodine deficiency syndrome, mixed form. Endemic cretinism, mixed form
- E00.9 Congenital iodine deficiency syndrome, unspecified Congenital hypothyroidism due to iodine deficiency NOS. Endemic cretinism NOS
- E01 Diseases of the thyroid gland associated with iodine deficiency and related conditions. Excluded: congenital iodine deficiency syndrome (E.00-), subclinical hypothyroidism due to iodine deficiency (E02)
- E01.0 Diffuse (endemic) goiter associated with iodine deficiency
- E01.1 Multinodular (endemic) goiter associated with iodine deficiency Nodular goiter associated with iodine deficiency
- E01.2 Goiter (endemic) associated with iodine deficiency, unspecified Endemic goiter NOS
- E01.8 Other diseases of the thyroid gland associated with iodine deficiency and related conditions. Acquired hypothyroidism due to iodine deficiency NOS
- E02 Subclinical hypothyroidism due to iodine deficiency
- E03 Other forms of hypothyroidism.
- E03.0 Congenital hypothyroidism with diffuse goiter. Congenital goiter (non-toxic): NOS, parenchymal, Excluded: transient congenital goiter with normal function (P72.0)
- E03.1 Congenital hypothyroidism without goiter. Thyroid aplasia (with myxedema). Congenital: thyroid atrophy hypothyroidism NOS
- E03.2 Hypothyroidism due to drugs and other exogenous substances
- E03.3 Post-infectious hypothyroidism
- E03.4 Thyroid atrophy (acquired) Excluded: congenital atrophy of thyroid gland (E03.1)
- E03.5 Myxedema coma
- E03.8 Other specified hypothyroidism
- E03.9 Unspecified hypothyroidism Myxedema NOS
- E04 Other forms of non-toxic goiter.
- E04.0 Nontoxic diffuse goiter. Goiter non-toxic: diffuse (colloidal), simple
- E04.1 Nontoxic single nodular goiter. Colloid node (cystic), (thyroid). Non-toxic monodose goiter. Thyroid (cystic) node NOS
- E04.2 Nontoxic multinodular goiter. Cystic goiter NOS. Polydose (cystic) goiter NOS
- E04.8 Other specified non-toxic goiter
- E04.9 Non-toxic goiter, unspecified. Goiter NOS. Nodular goiter (non-toxic) NOS
- E05 Thyrotoxicosis [hyperthyroidism]
- E05.0 Thyrotoxicosis with diffuse goiter. Exophthalmic or toxic goiter. NOS. Graves' disease... Diffuse toxic goiter
- E05.1 Thyrotoxicosis with toxic single-nodular goiter. Thyrotoxicosis with toxic mononodose goiter
- E05.2 Thyrotoxicosis with toxic multinodular goiter. Toxic nodular goiter NOS
- E05.3 Thyrotoxicosis with ectopia of thyroid tissue
- E05.4 Artificial thyrotoxicosis
- E05.5 Thyroid crisis or coma
- E05.8 Other forms of thyrotoxicosis. Hypersecretion of thyroid-stimulating hormone
- E05.9 Thyrotoxicosis, unspecified Hyperthyroidism NOS. Thyrotoxic heart disease (I43.8 *)
- E06 Thyroiditis.
- E06.0 Acute thyroiditis Abscess of the thyroid gland. Thyroiditis: pyogenic, purulent
- E06.1 Subacute thyroiditis De Quervain's thyroiditis, giant cell, granulomatous, non-purulent. Excluded: autoimmune thyroiditis (E06.3)
- E06.2 Chronic thyroiditis with transient thyrotoxicosis.
- E06.3 Autoimmune thyroiditis Hashimoto's thyroiditis. Hasitotoxicosis (transient). Lymphadenomatous goiter. Lymphocytic thyroiditis. Lymphomatous struma
- E06.4 Drug-induced thyroiditis.
- E06.5 Chronic thyroiditis: NOS, fibrous, woody, Riedel
- E06.9 Thyroiditis, unspecified
- E07 Other diseases of the thyroid gland
- E07.0 Hypersecretion of calcitonin. C-cell hyperplasia of the thyroid gland. Hypersecretion of thyrocalcitonin
- E07.1 Dyshormonal goiter. Familial dyshormonal goiter. Pendred's Syndrome.
- E07.8 Other specified diseases of the thyroid gland. Defect in tyrosine-binding globulin. Hemorrhage, Heart attack in the thyroid gland.
- E07.9 Disease of thyroid gland, unspecified
Chronic autoimmune thyroiditis, autoimmune lymphocytic thyroiditis, Hashimoto's thyroiditis, lymphadenomatous goiter, lymphomatous struma.
Version: MedElement Disease Handbook
Autoimmune thyroiditis (E06.3)
Endocrinology
general information
Short description
Autoimmune thyroiditis- chronic inflammatory disease of the thyroid gland (TG) of autoimmune genesis, in which, as a result of chronically progressive lymphoid infiltration, gradual destruction of the thyroid tissue occurs, most often leading to the development of primary hypothyroidism Hypothyroidism is a thyroid insufficiency syndrome characterized by neuropsychiatric disorders, edema of the face, limbs and trunk, bradycardia
.
The disease was first described by the Japanese surgeon H. Hashimoto in 1912. It develops more often in women after 40 years. There is no doubt about the genetic condition of the disease, which is realized under the influence of environmental factors (long-term intake of excess iodine, ionizing radiation, the effect of nicotine, interferon). The hereditary genesis of the disease is confirmed by the fact of its association with certain antigens of the HLA system, more often with HLA DR 3 and DR 5.
Classification
Autoimmune thyroiditis (AIT) is subdivided into:
1. Hypertrophic AIT(Hashimoto's goiter, classic version) - an increase in the volume of the thyroid gland is characteristic, histologically in the thyroid tissue, massive lymphoid infiltration with the formation of lymphoid follicles, oxyphilic transformation of thyrocytes is revealed.
2. Atrophic AIT- a decrease in the volume of the thyroid gland is characteristic, signs of fibrosis predominate in the histological picture.
Etiology and pathogenesis
Autoimmune thyroiditis (AIT) develops against the background of a genetically determined defect in the immune response, leading to T-lymphocytic aggression against one's own thyrocytes, resulting in their destruction. The genetic dependence of development is confirmed by the fact of the association of AIT with certain antigens of the HLA system, more often with HLA DR 3 and DR 5.
In 50% of cases, circulating antibodies to the thyroid gland are found in relatives of patients with AIT. In addition, there is a combination of AIT in the same patient or within the same family with other autoimmune diseases - type 1 diabetes, vitiligo Vitiligo - idiopathic skin dyschromia, characterized by the appearance of depigmented spots of various sizes and outlines of a milky white color with an area of \u200b\u200bmoderate hyperpigmentation surrounding them
, pernicious anemia, chronic autoimmune hepatitis, rheumatoid arthritis, etc.
The histological picture is characterized by lymphocytic and plasmacytic infiltration, oncocytic transformation of thyrocytes (formation of Gürtle-Ashkenazi cells), destruction of follicles and proliferation Proliferation - an increase in the number of cells of any tissue due to their multiplication
fibrous (connective) tissue, which replaces the normal structure of the thyroid gland.
Epidemiology
It occurs in women 4-6 times more often than in men. The ratio of persons aged 40-60 years suffering from autoimmune thyroiditis between men and women is 10-15: 1.
Among the population of various countries, AIT occurs in 0.1-1.2% of cases (in children), in children there is one boy for every 3 sick girls. AIT is rare in children under 4 years of age; the maximum incidence occurs in the middle of puberty. In 10-25% of practically healthy individuals with euthyroidism Euthyroidism - normal functioning of the thyroid gland, no symptoms of hypo- and hyperthyroidism
anti-thyroid antibodies can be detected. The incidence is higher in individuals with HLA DR 3 and DR 5.
Factors and risk groups
At-risk groups:
1. Women over 40 years of age, with a hereditary predisposition to thyroid diseases, or in the presence of such in the next of kin.
2. Individuals with HLA DR 3 and DR 5. Atrophic variant of autoimmune thyroiditis is associated with a haplotype Haplotype - a set of alleles at the loci of the same chromosome (different forms of the same gene located in the same regions), usually inherited together
HLA DR 3, and the hypertrophic variant with DR 5 HLA-system.
Risk factor:long-term intake of large doses of iodine with sporadic goiter.
Clinical picture
Symptoms, course
The disease develops gradually - over several weeks, months, sometimes years.
The clinical picture depends on the stage of the autoimmune process, the degree of damage to the thyroid gland.
Euthyroid phase can last for many years or decades, or even throughout a lifetime.
Further, as the process progresses, namely, gradual lymphocytic infiltration of the thyroid gland and destruction of its follicular epithelium, the number of cells producing thyroid hormones decreases. Under these conditions, in order to provide the body with a sufficient amount of thyroid hormones, the production of TSH (thyroid stimulating hormone) increases, which hyperstimulates the thyroid gland. Due to this hyperstimulation for an indefinite time (sometimes tens of years), it is possible to maintain T 4 production at a normal level. it phase of subclinical hypothyroidism, where there are no obvious clinical manifestations, but the TSH level is increased at normal T 4 values.
With further destruction of the thyroid gland, the number of functioning thyrocytes falls below the critical level, the concentration of T 4 in the blood decreases and hypothyroidism manifests itself phase of overt hypothyroidism.
Quite rarely, AIT can manifest transient thyrotoxic phase (hashi toxicosis)... The cause of hashi toxicosis can be both destruction of the thyroid gland and its stimulation due to the transient production of stimulating antibodies to the TSH receptor. Unlike thyrotoxicosis in Graves' disease (diffuse toxic goiter), hashi toxicosis in most cases does not have a pronounced clinical picture of thyrotoxicosis and proceeds as subclinical (decreased TSH at normal values \u200b\u200bof T 3 and T 4).
The main objective sign of the disease is goiter(enlargement of the thyroid gland). Thus, the main complaints of patients are associated with an increase in the volume of the thyroid gland:
- a feeling of difficulty swallowing;
- difficulty breathing;
- often a slight pain in the thyroid gland.
When hyperthroic formThe thyroid gland is visually enlarged, on palpation it has a dense, heterogeneous ("uneven") structure, not welded to the surrounding tissues, painless. Sometimes it can be regarded as a nodular goiter or thyroid cancer. Tension and slight tenderness of the thyroid gland can be noted with a rapid increase in its size.
When atrophic formthe volume of the thyroid gland is reduced, palpation is also determined by heterogeneity, moderate density, with the surrounding tissues of the thyroid gland is not welded.
Diagnostics
Diagnostic criteria for autoimmune thyroiditis include:
1. Increased levels of circulating antibodies to the thyroid gland (antibodies to thyroid peroxidase (more informative) and antibodies to thyroglobulin).
2. Detection of typical ultrasound data of AIT (diffuse decrease in the echogenicity of thyroid tissue and an increase in its volume in hypertrophic form, in atrophic form - a decrease in thyroid volume, usually less than 3 ml, with hypoechoicity).
3. Primary hypothyroidism (overt or subclinical).
In the absence of at least one of the listed criteria, the diagnosis of AIT is probabilistic.
Puncture biopsy of the thyroid gland to confirm the diagnosis of AIT is not indicated. It is carried out for differential diagnosis with nodular goiter.
After establishing the diagnosis, further study of the dynamics of the level of circulating antibodies to the thyroid gland in order to assess the development and progression of AIT has no diagnostic and prognostic value.
In women planning pregnancy, if antibodies to thyroid tissue and / or ultrasound signs of AIT are detected, it is necessary to examine thyroid function (determination of the level of TSH and T4 in the blood serum) before conception, as well as in each trimester of pregnancy.
Laboratory diagnostics
1. Complete blood count: normo- or hypochromic anemia.
2. Biochemical blood test: changes characteristic of hypothyroidism (increased levels of total cholesterol, triglycerides, moderate increase in creatinine, aspartate transaminase).
3. Hormonal research: various variants of thyroid dysfunction are possible:
- an increase in the level of TSH, the content of T 4 within the normal range (subclinical hypothyroidism);
- an increase in the level of TSH, a decrease in T 4 (manifest hypothyroidism);
- a decrease in the level of TSH, the concentration of T 4 within the normal range (subclinical thyrotoxicosis).
Without hormonal changes in thyroid function, the diagnosis of AIT is not valid.
4. Detection of antibodies to thyroid tissue: as a rule, there is an increase in the level of antibodies to thyroperoxidase (TPO) or thyroglobulin (TG). A simultaneous rise in the titer of antibodies to TPO and TG indicates the presence or high risk of autoimmune pathology.
Differential diagnosis
Differential diagnostic search for autoimmune thyroiditis should be carried out depending on the functional state of the thyroid gland and the characteristics of the goiter.
The hyperthyroid phase (hashi-toxicosis) should be differentiated from diffuse toxic goiter.
In favor of autoimmune thyroiditis are evidenced by:
- the presence of an autoimmune disease (in particular, AIT) in close relatives;
- subclinical hyperthyroidism;
- moderate severity of clinical symptoms;
- a short period of thyrotoxicosis (less than six months);
- no increase in the titer of antibodies to the TSH receptor;
- typical ultrasound picture;
- rapid achievement of euthyroidism with the appointment of small doses of thyreostatics.
The euthyroid phase should be differentiated from diffuse non-toxic (endemic) goiter (especially in areas with iodine deficiency).
The pseudo-nodular form of autoimmune thyroiditis is differentiated from nodular goiter, thyroid cancer... Puncture biopsy in this case is informative. A typical morphological sign for AIT is a local or widespread infiltration of thyroid tissue by lymphocytes (lesions consist of lymphocytes, plasma cells and macrophages, there is a penetration of lymphocytes into the cytoplasm of acinar cells, which is not typical for the normal structure of the thyroid gland), as well as the presence of large oxyphilic Gyurtle cells. Ashkenazi.
Complications
The only clinically significant problem that AIT can lead to is hypothyroidism.
Treatment abroad
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Treatment
Treatment goals:
1. Compensation of thyroid function (maintenance of TSH concentration in the range of 0.5 - 1.5 mIU / L).
2. Correction of disorders associated with an increase in the volume of the thyroid gland (if any).
Currently, it is recognized as ineffective and inappropriate to use sodium levothyroxine in the absence of violations of the functional state of the thyroid gland, as well as glucocorticoids, immunosuppressants, plasmapheresis / hemosorption, laser therapy in order to correct antithyroid antibodies.
The dose of levothyroxine sodium required for replacement therapy for hypothyroidism in the presence of AIT is on average 1.6 μg / kg of body weight per day or 100-150 μg / day. Traditionally, when choosing an individual therapy, L-thyroxine is prescribed starting from relatively low doses (12.5-25 μg / day), gradually increasing them until the euthyroid state is reached.
Levothyroxine sodium orally in the morning on an empty stomach, for 30 minutes. before breakfast, 12.5-50 mcg / day, followed by an increase in the dose by 25-50 mcg / day. up to 100-150 mcg / day. - for life (under the control of the TSH level).
A year later, an attempt was made to discontinue the drug in order to exclude the transient nature of thyroid dysfunction.
The effectiveness of therapy is assessed by the level of TSH: with the appointment of a full replacement dosage - after 2-3 months, then once every 6 months, then once a year.
According to the clinical guidelines of the Russian Association of Endocrinologists, physiological doses of iodine (about 200 μg / day) do not have a negative effect on thyroid function in case of pre-existing hypothyroidism caused by AIT. When prescribing preparations containing iodine, one should remember about a possible increase in the need for thyroid hormones.
In the hyperthyroid phase of AIT, thyreostatics should not be prescribed, it is better to do with symptomatic therapy (β-blockers): propronolol 20-40 mg orally 3-4 times a day, until the clinical symptoms are eliminated.
Surgical treatment is indicated with a significant increase in the thyroid gland with signs of compression of the surrounding organs and tissues, as well as with a rapid increase in the size of the thyroid gland against the background of a long-term moderate increase in the thyroid gland.
Forecast
The natural course of autoimmune thyroiditis is the development of persistent hypothyroidism, with the appointment of lifelong hormone replacement therapy with sodium levothyroxine.
The likelihood of developing hypothyroidism in a woman with an elevated level of AT-TPO and a normal level of TSH is about 2% per year, the likelihood of developing overt hypothyroidism in a woman with subclinical hypothyroidism (TSH is increased, T 4 is normal) and an increased level of AT-TPO is 4.5 % in year.
In women who are carriers of AT-TPO without dysfunction of the thyroid gland, with the onset of pregnancy, the risk of developing hypothyroidism and the so-called gestational hypothyroxinemia increases. In this regard, in such women, it is necessary to monitor thyroid function in the early stages of pregnancy, and, if necessary, at later stages.
Hospitalization
The term of inpatient treatment and examination for hypothyroidism is 21 days.
Prevention
There is no prophylaxis.
Information
Sources and Literature
- Braverman L. Diseases of the thyroid. - Humana Press, 2003
- Balabolkin M.I., Klebanova E.M., Kreminskaya V.M. Differential diagnosis and treatment of endocrine diseases. Guide, M., 2002
- pp. 258-270
- Dedov I.I., Melnichenko G.A. Endocrinology. National Leadership, 2012.
- pp. 515-519
- Dedov I.I., Melnichenko G.A., Gerasimov G.A. and other Clinical guidelines of the Russian Association of Endocrinologists for the diagnosis and treatment of autoimmune thyroiditis in adults. Clinical Thyroidology, 2003
- Vol. 1, pp. 24-25
- Dedov I.I., Melnichenko G.A., Andreeva V.N. Rational pharmacotherapy of endocrine system diseases and metabolic disorders. A guide for practicing physicians, M., 2006
- pp. 358-363
- Dedov I.I., Melnichenko G.A., Pronin V.S. Clinical picture and diagnosis of endocrine disorders. Teaching aid, M., 2005
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Chronic autoimmune thyroiditis - thyroiditis, usually manifested by goiter and symptoms of hypothyroidism. The risk of malignancy of the thyroid gland is slightly increased, but it cannot be said about a significant increase. The predominant age is 40-50 years. In women, it is observed 8-10 times more often.
Code for the international classification of diseases ICD-10:
Causes
Etiology and pathogenesis ... An inherited defect in the function of T - suppressors (140300, association with loci DR5, DR3, B8, B) leads to stimulation of the production of cytostimulating or cytotoxic antibodies by T - helpers to thyroglobulin, the colloidal component and the microsomal fraction with the development of primary hypothyroidism, an increase in TSH production, and ultimately the result is a goiter. Depending on the predominance of the cytostimulating or cytotoxic effect of AT, hypertrophic, atrophic and focal forms of chronic autoimmune thyroiditis are distinguished. Hypertrophic. Association with HLA - B8 and - DR5, predominant production of cytostimulating antibodies .. Atrophic. Association with HLA - DR3, preferential production of cytotoxic antibodies, resistance of receptors to TSH .. Focal. The defeat of one lobe of the thyroid gland. The AT ratio can be different.
Pathological anatomy... Abundant infiltration of the gland stroma with lymphoid elements, incl. plasma cells.
Symptoms (signs)
Clinical picture is determined by the ratio of cytostimulating or cytotoxic antibodies. An enlarged thyroid gland is the most common clinical manifestation. Hypothyroidism by the time of diagnosis is found in 20% of patients, but in some it develops later. During the first months of the disease, hyperthyroidism can be observed.
Diagnostics
Diagnostics ... Ultrasound - characteristic signs of AIT (heterogeneity of the structure of the thyroid gland, decreased echogenicity, thickening of the capsule, sometimes calcifications in the tissue of the gland). High titers of antithyroglobulin or antimicrosomal antibodies. Thyroid function test results vary.
Diagnostic tactics... AIT is diagnosed only if there are three signs:. hypothyroidism. characteristic changes during ultrasound. high titer of AT to Ar of the thyroid gland (thyroglobulin and thyroid peroxidase).
Treatment
TREATMENT
Drug therapy
According to current recommendations, thyroxine treatment is indicated only in the presence of hypothyroidism, clinically and laboratory confirmed. Levothyroxine sodium at an initial dose of 25 or 50 mcg / day with further correction until the serum TSH content decreases to the lower limit of the norm.
Tiamazole, propranolol - with clinical manifestations of hyperthyroidism.
Comorbidity... Other autoimmune diseases (for example, B 12 deficiency anemia or rheumatoid arthritis).
Synonyms ... Hashimoto's disease. Hashimoto's goiter. Hashimoto's thyroiditis. Lymphomatous goiter. Lymphadenoid goiter. The blastoma of the thyroid gland is lymphadenoid. The goiter is lymphocytic.
ICD-10 . E06.3 Autoimmune thyroiditis
The ICD 10 code is the name of a disease in the worldwide classification of diseases. The ICD is a huge system that was created in order to study diseases in detail and track the trend in the incidence of the population. This classification was adopted more than a century ago in Paris, however, it is changed and supplemented every 10 years.
The code under the code ten appeared in 1993 and characterized a thyroid disease, namely. The meaning of the ICD was to identify complex pathologies and carry out diagnostics, which were subsequently compared in many countries of the world. Thanks to this classification, an optimal system for the treatment of all pathologies has been developed. Each has its own code according to the ICD 10 system.
Generally accepted structure of ICD 10
All disease information has been compiled in such a way that it can be used to compile the most useful database. The ICD 10 code contains the following pathologies:
- diseases of an epidemic nature;
- common diseases;
- diseases associated with anatomical localization;
- developmental pathology;
- various types of injuries.
The code contains over twenty groups. Autoimmune thyroiditis is contained in the group of thyroid dysfunction and includes the following disease codes:
- acute, which is designated by the code E06.0 - it is characterized by a thyroid abscess and is divided into purulent and pyogenic. Sometimes other codes are applied to it, namely B95, B96, B97;
- has encryption E06.1 and is divided into de Quervain's thyroiditis, giant (cellular), granular and without pus;
- chronic often turns into thyrotoxicosis and is designated as E06.2;
- autoimmune, which is divided into 4 subspecies: Hashimoto's disease Hasitotoxicosis (also called transient), lymphadenomatous goiter, lymphocytic thyroiditis, lymphomatous struma;
- medicinal, encrypted as E06.4, but other encodings are used if necessary;
- ordinary, which includes chronic, woody, fibrious, Riedel's thyroiditis and NOS. Bears code E06.5;
- unspecified, code E06.9.
Characteristics of the subspecies of autoimmune thyroiditis ICD 10
Hashimoto's disease is a pathology that occurs when hormone levels fall rapidly, which occurs due to a reduction in the volume of hormone-producing tissue.
Riedel's disease, or as it is also called fibrious, is chronic. Its feature is the replacement of the parenchyma with another type of tissue (connective).
And if the Hashimoto subspecies appears very often, then the Riedel subspecies, on the contrary, is very rare.
With the first disease, the disease mainly affects women over the age of thirty-five. It appears like this: the normal tissues of the thyroid gland disintegrate, and new ones appear in their place.
In other words, due to autoimmune aggression, diffuse infiltration of the thyroid gland by lymphocytes occurs with the formation of lymphoid follicles (lymphocytic thyroiditis), destruction of thyrocytes and proliferation of fibrous tissue.
The transition phase of hyperthyroidism is closely interrelated with the non-functionality of healthy epithelial cells of the follicle and the ingestion of long-synthesized hormones into the human blood. In the future, this leads to the occurrence of hypothyroidism.
In the second subspecies of the disease, the healthy parenchyma changes to fibrious tissue, which causes the compression syndrome. This type is very often interconnected with different types of fibriosis, namely mediastinal and retroperitoneal, which makes it possible to study it within the framework of Ormond's systemic fibrosing syndrome. There is an opinion that Riedel's thyroiditis is the outcome of Hashimoto's thyroiditis.
Hashimoto's disease is divided into two forms of pathology development - hypertrophic and atrophic. The first form is explicit, and the second is latent.
Diagnosis and treatment of autoimmune thyroiditis
First of all, you need to conduct an examination for Hashimoto's thyroiditis when the following symptoms appear in a woman aged 35-40 years:
- hair began to fall out;
- breaking nails;
- face swelling appears;
- dry skin.
To do this, you need to donate blood for T and TSH analysis. And also the doctor determines by touch whether the lobes of the thyroid gland are enlarged and they are asymmetric or not. When conducting an ultrasound examination, the general picture of the disease is very similar to DTZ - the tissue has many layers and pseudo-nodes.
If Riedel is diagnosed, then the thyroid gland will be very dense and involve neighboring organs in the disease. This disease is difficult to distinguish from thyroid cancer.
With autoimmune thyroiditis, the ICD code 10 is prescribed lifelong hormone therapy. The operation is prescribed in individual cases (large goiter, malignant tumor).